|Institution:||University of British Columbia|
|Full text PDF:||http://hdl.handle.net/2429/50318|
Background: Deaths from exsanguination following trauma remain a clinical challenge. Current massive transfusion protocols embrace empiric resuscitation with packed red blood cells, plasma and platelets in a set ratio. With the evolving knowledge about acute traumatic coagulopathy (ATC) as a major contributor to exsanguination related deaths, it is apparent that current resuscitation protocols may fail to address the early coagulation deficits in trauma. Objective: To provide a review of the current literature related to the pathophysiology of ATC in order to guide clinicians in optimizing diagnostic and therapeutic strategies in massively bleeding trauma patients. Methods: Online search from the Medline database of all published articles since 2003 till March 2014. Results: Initial search resulted in 20,504 articles of which 54 were included. Principle findings include: (1) Activated protein C is strongly linked to ATC pathophysiology and related to shock and tissue injury. (2) FV is commonly depleted, but thrombin generation is preserved, potentially minimizing the role of FV in ATC. (3) Hypofibrinogenaemia occurs very early in trauma and is strongly associated with higher mortality. A lower threshold for administration of fibrinogen-containing products should therefore be considered. (4) Hyperfibrinolysis incidence is low but is associated with increased transfusion requirements and higher mortality. Fibrinolytic activation is evident in almost half of trauma patients and is associated with higher injury severity score and higher mortality compared to patients with no fibrinolytic activation. (5) Platelet dysfunction plays a more important role in ATC pathophysiology compared to platelet counts. (6) Endothelial damage and sympathoadrenal activation are associated with glycocalyx degradation, higher adrenaline levels and autoheparinization, all contributing to the bleeding diathesis in trauma. Conclusion: ATC is a complex endogenous state of hypo-coaguloability in shocked and severely injured trauma patients and is associated with increased transfusion requirements and higher mortality. Early fibrinogen depletion and fibrinolysis appears to play a central role in ATC and modification of current empiric resuscitation protocols in order to address these hemostatic deficits is needed. New knowledge of ATC is rapidly expanding, requiring regular reviews and knowledge dissemination to inform clinicians and guide appropriate management of ATC.